Shiva Malek

Figure S1 from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

<p>Taselisib and GDC-0077 have increased potency in PIK3CA-mutant cancer cells</p>

Figure S4 from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

<p>Taselisib depletes mutant p110a protein through ubiquitin and proteasome mechanism in a dose and time dependent manner</p>

Figure S3 from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

<p>Taselisib and GDC-0077 induce mutant p110a and not WT p110a degradation</p>

Figure S6 from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

<p>RTK activity plays a key role in regulating p110a degradation</p>

RAF inhibitors prime wild-type RAF to activate the MAPK pathway and enhance growth

Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have broad therapeutic...

RAS-targeted therapies: is the undruggable drugged?

Figure S5 from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

<p>Taselisib-mediated degradation of mutant p110a occurs preferentially at the plasma membrane.</p>

Figure S2 from RTK-Dependent Inducible Degradation of Mutant PI3Kα Drives GDC-0077 (Inavolisib) Efficacy

<p>Activity of GDC-0077 in combination with Palbociclib and/ or Fulvestrant</p>